[unreadable] My research will investigate both the functional development of the auditory cortex (ACx), as well as any disruptions posed by early-life chronic nicotine exposure (CNE). Since hearing onset occurs during postnatal development in rats (p12), we can study the physiology of ACx neurons from the first day of hearing in vivo. Therefore, any functional deficiencies in the ACx from developmental nicotine exposure can be monitored in several different manners. First, I plan to record frequency receptive fields from the ACx of young (p13-19) CNE and control rats using both local field potentials and single units (loose-patch). These experiments will determine if CNE impairs frequency tuning in the ACx during an important period for cortical plasticity. Next, I will study how CNE affects synaptic and glutamatergic NMDA receptor maturation in the ACx using both pharmacological and physiological manipulations. Intracortical infusions of NMDAR antagonists (APV and ifenprodil) while recording from the ACx of nicotine treated and control rats will determine the role of NMDARs in receptive field generation. Also, in vivo whole-cell voltage clamp recordings will be conducted to examine how cortical excitation and inhibition develop in both normal and CNE animals, as well as to investigate the existence of pure-NMDAR synapses ("silent synapses") in the developing ACx. [unreadable] [unreadable] [unreadable] [unreadable] [unreadable]